AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

René Laennec, inventor of the stethoscope, first described bronchiectasis in 1819 while observing patients with tuberculosis and the sequelae of pneumonia in the preantibiotic era. The term bronchiectasis is derived from the Greek bronchion, meaning windpipe, and ektasis, meaning stretched. Bronchiectasis is characterized by the dilatation of bronchi with destruction of elastic and muscular components of their walls. Bronchiectasis can be focal or diffuse. It is usually due to acute or chronic infection, anatomic airway obstruction, or underlying congenital disease that predisposes to chronic infection.

The presentation includes recurrent respiratory infections, productive cough, shortness of breath, and occasional hemoptysis. In the developed world, immunizations and antibiotics have led to a declining incidence. In these countries, diffuse bronchiectasis is more often found in association with underlying disorders such as cystic fibrosis (CF), immune deficiencies (including human immunodeficiency virus [HIV]), primary ciliary dyskinesia, and recurrent aspiration syndromes. Focal bronchiectasis is usually associated with bronchial obstruction (ie, foreign body) that leads to infection. In developing countries, bronchiectasis is still frequently encountered as one of the sequelae of acute infection.

Pathophysiology

Bronchiectasis generally results from obstruction and inflammation of the airway. The obstruction and inflammation may result from any of the underlying disorders listed above or from infection with acute tuberculosis, adenovirus, measles, Mycobacterium avium, or Aspergillus fumigatus.

The damage may result from chronic infection that leads to recruitment of neutrophils, T lymphocytes, and monocyte-derived cytokines. The release of inflammatory mediators, elastases, and collagenases leads to inflammation and destruction of elastic and muscular components of bronchial walls. In addition, the outward elastic recoil forces of surrounding lung parenchyma exert traction, which causes expansion of airway diameter. These changes may be accompanied by bronchial arterial proliferation, which predisposes to hemoptysis.

Bronchiectasis associated with bronchial obstruction may have a focal distribution distal to the site of obstruction. Bronchiectasis associated with underlying disease is likely to be diffuse.

Frequency

United States

Current population-based estimates of occurrence are not available. In 1963, Clark estimated an incidence of 1.06 cases per 10,000 population. The incidence of bronchiectasis associated with underlying systemic disease reflects the incidence of the particular disease. The most common congenital disease associated with bronchiectasis is CF.

International

In developed countries, the frequency is similar to that in the United States. The frequency is higher in the developing world, where measles, pneumonia, tuberculosis, and HIV infection are all on the rise and are associated with bronchiectasis. Childhood national rates have been reported out of London, Finland, New Zealand, and Alaska.

• Starting in 1949, Field studied children with bronchiectasis in London for almost 2 decades and documented a fall in the annual hospitalization rate for bronchiectasis in 5 British hospitals, from approximately 48 cases per 10,000 population to 10 cases per 10,000 population (Field, 1969).
• Twiss et al (2005) reported the incidence of bronchiectasis in children younger than 15 years is 3.7 per 100,000 population. The incidence is highest among children who live in Pacific regions at 17.8 per 100,000 population. The incidence is 4.8 per 100,000 population in Maori and 1.5 per 100,000 in New Zealand compared with 2.4 per 100,000 in other Pacific regions. The incidence of bronchiectasis in New Zealand children is nearly twice the rate of CF and 7 times that of Finland. They found variations in incidence among ethnic groups. Most New Zealand children with bronchiectasis developed disease in early childhood and had a delayed diagnosis.
• Callahan et al (2005) reported the incidence among Alaskan Native children in the Yuskon-Kuskokwim region to be about 140 cases per 10,000 population, compared with 1 per 10,000 in other continental US studies. Redding et al (2004) reported the incidence of bronchiectasis in southwest Alaskan Natives is 16 per 1,000 population.
• In central Australian aborigines, the incidence is 14 per 1,000 population, compared with 0.1 per 1,000 in Scotland and 4.9 per 1,000,000 in Finnish children (Redding, 2004).

Mortality/Morbidity

Limited morbidity and mortality data are available.

• In Field's original group, who were studied at the beginning of the antibiotic era, 4% of children with medically treated bronchiectasis died (9-10 from infection), and 3% of children who were surgically treated died (8-9 immediately following or as a late result of surgery) in the ensuing 2 decades.
• Karadag et al (2005) illustrated that bronchiectasis remains one of the most common causes of childhood morbidity in developing countries.
• Twiss et al recently demonstrated that children with bronchiectasis have significant airway obstruction that deteriorates over time. However, Karadag et al demonstrated that children with CF have a more rapid decline in forced expiratory volume at one second (FEV₁) than children with non-CF bronchiectasis.
• Akalin et al reported decreased left ventricular function and exercise capacity in bronchiectasis. In children with CF, ventilation perfusion mismatch and hypoxemia may result in cor pulmonale.

Race

Bronchiectasis is more common in patients of Polynesian and Alaskan Native ancestry. In a survey of 26,000 Samoans in Western Samoa, the prevalence of bronchiectasis was 0.6%, probably the highest of any population in the world. Karadag's study in Turkey suggests possible genetic predisposition in some populations and found that 43% of children with bronchiectasis had parents who were first- or second-degree relatives.

Sex

Morrissey et al found non-CF bronchiectasis to be more common and more virulent in women.

Age

• Karadag et (2005) reported a mean age at presentation of 7.4 ±3.7 years. In a survey of newborns diagnosed with CF, Farrell et al found potentially irreversible abnormalities in one half of the children by age 2 years.
• In Field's 1949 survey, 15% of patients presented when younger than 2 years, 43% when aged approximately 2 years, and 92% when younger than 10 years. These data predate most current immunizations and antibiotics.
• In Clark's 1963 series, one half of the children developed symptoms when younger than 3 years.

CLINICAL

Section 3 of 10  

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• Clinical
• Workup
• Treatment
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• Miscellaneous
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History

• Cough
• • Non-CF bronchiectasis in children presents with a wide spectrum of disease severity. Some children have intermittent symptoms of cough and occasional lower respiratory tract infections. Others experience daily cough and produce purulent fetid sputum, requiring frequent hospitalizations for respiratory exacerbations.
  • The diagnosis should be considered in children with a daily productive cough for longer than 6 weeks.
  • Recurrent cough with fetid sputum, hemoptysis, or recurrent pneumonia are important clues to early diagnosis of this disease.
  • Cough is an almost universal symptom and is frequently described as productive in older children or loose in toddlers and infants. Because small children rarely expectorate, the clinician may observe the child with a loose-sounding cough who swallows after coughing.
  • While cough is a cardinal symptom in bronchiectatic disease, Smyrnios et al concluded that cough is much more common in patients with asthma (24%), gastroesophageal reflux disease (GERD) (15%), and bronchitis (11%) than in patients with bronchiectasis (4%).
• Other
• • Tsao et al (2002) reported hemoptysis to be the second most common symptom of bronchiectasis.
  • The diagnosis of asthma or reflux-associated lung disease does not preclude bronchiectasis. In fact, bronchiectasis may be a complication of these diseases.
  • An underlying systemic disease or congenital anatomical malformations such as tracheoesophageal fistula or history of foreign body aspiration in conjunction with respiratory symptoms should increase suspicion for bronchiectasis.

Physical

• Physical examination findings in patients with bronchiectasis may include variable degrees of crackles or coarse rhonchi and clubbing. However, the examination findings may be normal. Lai et al (2004) reported crackles and wheezing as the most frequent findings of the physical examination.
• Digital clubbing is reported in 37-51% of patients with bronchiectasis. Edwards et al (2003) found that children with digital clubbing and chest deformity showed significantly higher scores for extent of bronchiectasis, bronchial wall dilatation and thickness, and overall changes based on CT score. In Field's 1949 series, clubbing was present in 78 cases (43.7%). In many of her cases, the clubbing cleared after the affected section of the lung was surgically removed. In medically treated cases, clubbing often improved and, in some cases, disappeared despite persistent bronchographic evidence of bronchiectasis. Field concluded that clubbing in the absence of congenital heart disease signifies irreversible bronchiectasis. This concept is not universally held.

Causes

All causes share the same pathophysiologic pathway: ineffective pulmonary toilet and chronic or recurrent infection and inflammation. Common causes include the following:

• Severe pneumonia
• Measles, tuberculosis, pertussis, M avium, and A fumigatus infections
• Intrinsic airway luminal obstruction by bronchial foreign body or extrinsic compression by mass
• Chronic aspiration, which is associated with swallowing dysfunction, GERD, or tracheoesophageal fistula
• Congenital conditions, including CF, ciliary dyskinesia, Marfan syndrome, Bruton agammaglobulinemia, and congenital absence of bronchial muscle (Mounier-Kuhn syndrome) or cartilage (Williams-Campbell syndromes)
• Immunoglobulin A (IgA) and G (IgG) deficiencies and IgG subclass deficiencies, especially IgG2 deficiency
• Connective tissue disorders, including rheumatoid arthritis and systemic lupus erythematosus
• HIV infection
• Allergic bronchopulmonary aspergillosis
• Tracheal stenosis with impaired mucociliary clearance
• Severe tracheomalacia with impairment of mucociliary clearance
• Fibrosing lung diseases associated with sarcoidosis or idiopathic pulmonary fibrosis
• Persistent atelectasis

WORKUP

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Laboratory evaluation should include the following tests:
• • Sweat chloride
  • Immunoglobulin E (IgE) and serum precipitins for Aspergillus species, A fumigatus–specific IgE, sputum culture for fungus, and an aspergillus skin test
  • CBC count
  • Serum IgG, immunoglobulin M (IgM), and IgA
  • IgG subclasses
  • HIV test
  • Sputum culture or deep oropharyngeal swab in younger children
  • Antinuclear antibody and rheumatoid factor

Imaging Studies

• Because bronchiectasis is defined as an abnormal dilatation of airways, the diagnosis depends on radiographically or anatomically visualizing the typical changes.
• • Chest radiography: Obtain a routine posteroanterior and lateral chest radiograph. However, normal radiograph findings do not rule out bronchiectasis.
  • Computed tomography
    • The diagnosis is usually established using high-resolution CT (HRCT) scanning, which has a sensitivity and specificity of 90%.
    • The key feature on HRCT scanning is an enlarged internal bronchial diameter with bronchi that appear larger than the accompanying artery, called the signet sign. Other HRCT scan findings include the failure of the larger airways to taper while progressing to the lung periphery, air fluid levels in the dilated airways, and the identification of airways in the extreme lung periphery.
  • Gastroesophageal reflux disease
    • Evaluate patients suspected of having bronchiectasis for GERD, especially infants and young children.
    • Studies may include barium esophagraphy, gastric scintiscanning, and intraesophageal pH monitoring.
    • Suspicion of poor oromotor coordination should lead to a swallow study.

Procedures

• Fiberoptic bronchoscopy may help assess the caliber and appearance of the airways and provide bronchoalveolar lavage fluid for evidence of chronic aspiration or infection (cultures and WBC differential).
• Fluoroscopically guided selective bronchography, using water-soluble contrast media and performed by an experienced bronchoscopist, provides excellent anatomic definition. Bronchiectasis is classified on bronchography as cylindrical, varicose, or saccular, although these pathologic distinctions may have little clinical correlation in terms of severity or outcome. This study has been virtually eliminated by CT scanning.

Histologic Findings

Examination of the bronchoalveolar fluid reveals inflammatory cells. Hemosiderin-laden macrophages generally suggest nonacute bleeding. Lipid-laden macrophages suggest chronic aspiration but may also be observed in other forms of severe airway disease.

TREATMENT

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Medical Care

In addition to the treatment of an identified underlying disorder, pharmacotherapy may be used to enhance bronchodilation and to improve mucociliary clearance. Antibiotics can be used to prevent and treat recurrent infections. Secretions can be mobilized with chest physiotherapy and mucolytic agents. Occasionally, surgery may be considered. The goal of therapy is to mobilize secretions and to reduce the infectious and inflammatory load, thereby preventing progression of airway destruction.

Randomized trials of these treatment options lack proper control groups. The markers used to assess therapy effectiveness have included the volume of sputum production and the clearance of a radiolabeled aerosol from the lung. More meaningful studies that focus on measures such as rate of respiratory exacerbations and quality of life are needed.

• Anti-inflammatory agents: Randomized placebo-controlled trials of inhaled corticosteroids in patients with non-CF bronchiectasis showed no significant improvement in lung function. Inhaled corticosteroids may have a role in regulating the host response and halting inflammatory damage to the lung.
• Bronchodilators: Bronchodilators are indicated when bronchial hyperreactivity is evident and are used to improve ciliary beat frequency and, thus, facilitate mucus clearance. However, no randomized studies have validated their usefulness in the management of bronchiectasis. Furthermore, some patients with bronchiectasis experience paradoxic bronchoconstriction with beta-agonist therapy. This is likely secondary to loss of airway tone due to beta-agonist relaxation of bronchial smooth muscle superimposed on already weakened bronchial cartilage in the bronchiectatic airway. Therefore, assessing bronchodilator response before beginning such therapy is critical.
• Mucolytics: Mucolytic drugs aim to improve tracheobronchial clearance via alteration of sputum consistency. Recombinant DNase did not show significant benefit in non-CF bronchiectasis. Patients with CF respond well, with improvement in spirometry compared with a placebo group.
• Antibiotics
• • A Cochrane review revealed that long-term therapy with antibiotics is effective in reducing sputum volume and purulence but has limited impact on the frequency of exacerbations and the natural history of the disease process. Also, chronic antibiotic use may result in the emergence of resistant organisms.
  • Many clinicians treat bronchiectasis with prolonged oral antibiotics on a rotating basis. Broad-spectrum antibiotics can be given for a month, followed by a second broad-spectrum drug, followed by a third, and so forth. Another option is to use alternating antibiotics for 7-10 days, with antibiotic-free periods of 7-10 days between each course.
  • Davies et al suggested that long-term triweekly therapy with azithromycin can be helpful in patients with bronchiectasis. This has also been helpful in CF.
  • Rosen et al (2006), in a review of the literature, concluded that antibiotics are helpful during exacerbations of bronchiectasis, with the selection of agents based on culture results.
  • Inhaled tobramycin was associated with decreased Pseudomonas aeruginosa load in sputum, improved lung function, and fewer hospitalizations. However, Rosen et al (2006) concluded that inhaled tobramycin is not indicated in non-CF bronchiectasis.
• Chest physiotherapy: Manual and mechanical interventions such as chest percussion, vibration, postural drainage, cough-assist devices, and airway oscillation (ie, flutter) are used to facilitate mucous expectoration. The goal is to facilitate effective airway clearance.

Surgical Care

• Pulmonary segmental resection may be beneficial when damage is severe and well localized.
• Prior to the proliferation and availability of broad-spectrum antimicrobials both Field (1969) and Clark (1963) demonstrated a gradual symptomatic improvement of some children who did not undergo surgical therapy for bronchiectasis.
• In 1993, Lewiston recommended that surgery be delayed, unless symptomatically necessary, until the patient is aged 6-12 years because of the possibility for clinical improvement. Surgery is also delayed in children with stable disease that can be controlled with medical therapy.
• Otgun et al (2004), in a retrospective study, concluded that the decision for bronchiectasis surgery should be made in cooperation with the chest disease unit. Furthermore, anatomic localization of disease should be mapped with radiography and scintigraphic studies. Otgun et al found the morbidity and mortality rates to be within acceptable ranges. In unilateral bronchiectasis, total excision and pneumonectomy, as opposed to leaving residual disease, was found to be well tolerated and most beneficial to the child.

Consultations

• Routine care of children with bronchiectasis is successfully provided by a primary care physician.
• A pediatric pulmonologist should be initially consulted for all infants and children with bronchiectasis.

Activity

• No specific activity limitations are necessary.
• Exercise generally promotes increased mucociliary clearance, which may enhance airway clearance in patients with bronchiectasis. However, exercise-induced dyspnea may require further investigation using exercise testing to evaluate for limitation or hypoxemia.

MEDICATION

Section 6 of 10  

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• References

Treatment for bronchiectasis consists of antibiotics for infections and bronchodilators for any airway hyperreactivity. Antibiotic therapy agents should be tailored to the results of sputum culture.

Increasingly, anti-inflammatory agents are prescribed, such as inhaled or oral corticosteroids. Nebulized albuterol has the added benefit of hydration in the nebulized form.

Drug Category: Corticosteroids, inhaled

These agents may be beneficial in treating chronic inflammation in bronchiectasis. They elicit anti-inflammatory and immunosuppressive properties and cause profound and varied metabolic effects. They also modify the body's immune response to diverse stimuli.

Drug Category: Bronchodilators

These act to decrease muscle tone in the small and large airways in the lungs, thereby increasing ventilation.

Drug Category: Antibiotics

Systemic and inhaled antibiotics are used in bronchiectatic disease to prevent or treat exacerbations caused by bacterial colonization that result in airway inflammation and injury. Antibiotics are generally chosen based on organisms and sensitivities from sputum cultures. The antibiotics used more commonly are listed below.

Drug Category: Inhaled antibiotics

These agents are indicated in bronchiectasis, specifically in patients with CF for P aeruginosa–positive sputum cultures.

FOLLOW-UP

Section 7 of 10  

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Further Inpatient Care

• Children may require inpatient intravenous antibiotics when they experience exacerbations of endobronchial disease. Exacerbation may be characterized by increased cough or sputum production or changes in pulmonary function. Nebulized antibiotics may be continued in children with CF.
• The initial course of treatment may be oral antibiotics and aggressive airway clearance. If the patient is unresponsive to oral antibiotics, intravenous antibiotic therapy and hospitalization may be necessary. Home intravenous antibiotic therapy may be an option in some situations.
• Systemic corticosteroids may be used to treat the reactive airway component, when appropriate.

Further Outpatient Care

• Children should be seen frequently, generally every 3-6 months. The interval may be lengthened as the clinical course dictates.
• Spirometry is recommended at every visit in children older than 5 years.
• Chest radiograph need not be empirically repeated. If the clinical course changes, a radiograph should be part of the assessment.

Transfer

• Consider transferring the care of the child with bronchiectasis to a pediatric pulmonary center if clinical deterioration, frequent or increased symptoms, or hemoptysis occurs.

Deterrence/Prevention

• Childhood immunization for measles or pertussis has reduced bronchiectasis in the developed world. Screening for tuberculosis and other successful public health measures minimizes the risk of this disease in children.
• Aggressive appropriate therapy of lower respiratory tract infections may prevent bronchiectasis. However, because some viruses predispose to bronchiectasis, this therapy is not always successful.

Complications

• Progressive bronchiectasis from underlying disease (CF) or ongoing pulmonary insult (aspiration syndromes) causes a progressive obstructive defect and, ultimately, respiratory compromise. This may manifest as dyspnea at rest or with exercise or sleep-disordered breathing.
• Progressive pulmonary damage may lead to cor pulmonale, hypercarbia, respiratory failure, and death.

Prognosis

• Overall, the prognosis is good for a child with bronchiectasis. The key to a successful outcome is determining whether the cause of the damage is ongoing (eg, chronic aspiration) and then treating the problem.
• Growth of new pulmonary tissue in children proceeds rapidly until about age 6 years and then tapers off through childhood. Injury at an early age may be compensated for by growth of normal healthy lungs in the absence of ongoing damage.
• Treating any underlying disorder can help prevent the progression of bronchiectasis. Chest drainage and antibiotics can help treat the bronchiectasis itself.
• In the absence of an underlying condition, children with isolated bronchiectasis have a good prognosis.

Patient Education

• Chest physiotherapy and postural drainage are important elements in the treatment of bronchiectasis and should be taught to the child's parents early in the course of disease. This is especially true when the child produces significant amounts of sputum. Physiotherapy techniques should be frequently reviewed and retaught.
• For excellent patient education resources, visit eMedicine's Bacterial and Viral Infections Center. Also, see eMedicine's patient education article Tuberculosis.

MISCELLANEOUS

Section 8 of 10  

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• Introduction
• Clinical
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• Treatment
• Medication
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• Miscellaneous
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• References

Medical/Legal Pitfalls

• Bronchiectasis is a relatively uncommon condition often unsuspected in a child with previously diagnosed obstructive pulmonary disease, such as asthma. The clinician must remember that asthma does not cause digital clubbing. A child with asthma and clubbing should be evaluated further.
• In patients with suspected bronchiectasis without characteristic chest radiograph findings, an HRCT scan is the diagnostic procedure of choice.
• Efforts should be made to determine any etiology of bronchiectasis.
• Children should be monitored throughout their lives by a clinician comfortable with the management of chronic lung disease.

Special Concerns

• In patients with CF, prolonged therapy with systemic corticosteroids may affect growth and increase the risk of diabetes.
• In patients with non-CF bronchiectasis, prolonged systemic antibiotics may produce a small benefit and reduce sputum volume and purulence but may also be associated with unpleasant side effects.

MULTIMEDIA

Section 9 of 10  

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• Miscellaneous
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Media file 1:  Posteroanterior chest radiograph of a child with bronchiectasis due to chronic aspiration.
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Media file 2:  CT scan of the chest of a child with bronchiectasis due to chronic aspiration.
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Media file 3:  Chest radiograph of a child with severe adenoviral pneumonia as an infant. The child has persistent symptoms of cough, congestion, and wheezing.
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Media file 4:  Bronchoscopic bronchogram of the left lower lobe on a patient with history of adenoviral pneumonia, demonstrating cylindrical and varicose types of bronchiectasis.
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Media type:  X-RAY

Media file 5:  Bronchoscopic bronchogram of the right upper lobe of a patient with a history of adenoviral pneumonia, demonstrating saccular bronchiectasis.
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Media type:  X-RAY

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
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• References

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Article Last Updated: Jan 22, 2007